Herpes simplex virus (HSV) types 1 and 2 cause infections of the skin and mucous membranes and can affect several organs, resulting in a variety of clinical manifestations, some of which can be very serious.

HSV-1 and HSV-2 are closely related and share common genetic material, but generally differ in their epidemiology.

Transmission of viral DNA can be the result of active virus being released by the host, often from infected lesions. Close contact is required for infection, because viral particles rarely survive outside the human body for long. HSV infection is a global, year-round problem.

1. Aetiology and pathogenesis

HSV can enter the body via damaged skin or through mucosa. The virus may be acquired by neuronal tissue, which enhances its ability to spread, as well as via local invasion and blood-borne routes.

After the initial infection has subsided, viral material may remain 'hidden' in nerve cells near the original infection site. Infection can be reactivated from this dormant state, which explains why some infections recur. What causes reactivation remains unclear but it somehow involves immune system responses.

However, reactivation can be associated with immunosuppression, a high temperature or stress, and many episodes and states of shedding active virus can remain unknown to the host.

This has implications for the rate of transmission and of course has significant meaning when dealing with HSV-2 (genital herpes).

2. Clinical features

Generally, HSV-1 is associated with oral and facial infections while HSV-2 is associated with genital lesions, although both virus types can result in infections in both areas.

When skin and mucosa are affected, the eyes, mouth or genitalia are also common sites of infection. In a first time infection, children and young adults are commonly affected. Owing to the intra-oral lesions (gingivostomatitis) caused by HSV, especially in a primary infection in children, there is a risk of reduced oral intake, potentially leading to dehydration.

A primary oral infection may cause no symptoms or it may lead to small blisters that can rupture and result in ulcers. Sometimes there are symptoms of infection - high temperature, swollen lymph nodes and general lethargy. Pharyngitis caused by HSV may be impossible to distinguish clinically from bacterial pharyngitis.

In patients with reduced immunity, herpetic lesions can be more invasive and longer lasting, and may spread more easily to other organs.

Herpes labialis (cold sores) is usually a reactivation of dormant HSV and is associated with typical lip lesions. Herpetic whitlow is an infection of the finger end, as virus is transmitted directly where the skin barrier has been breached.

A first or primary genital herpes infection can cause numerous painful genital ulcers; there may be associated regional lymphadenopathy. In the healing phase, lesions eventually form crusts.

Symptomless primary infection can happen but is uncommon. Retention of urine (from involvement of sacral innervations) and aseptic meningitis are possible complications.

Recurrence is relatively common but can be less severe than the original infection.

Herpes simplex encephalitis is a serious condition and neurological complications are relatively common. Neonatal herpes simplex infections can result in high morbidity, while infection of the corneal epithelium can lead to ulceration, causing symptoms such as photophobia.

Key points

HSV infection is a global, year-round problem.

Generally, HSV-1 is associated with oral and facial infections, while HSV-2 is associated with genital lesions.

In patients with reduced immunity, herpetic lesions can be more invasive and longer lasting, and spread more easily to other organs.

Recurrence is relatively common but can be less severe than the original infection.

Ensure patients are aware that they are potentially infectious when lesions are visible and that they can shed virus even in the absence of symptoms.

3. Investigations

HSV can be diagnosed by a combination of clinical and laboratory features. Where there are typical lesions, it is reasonable to make the diagnosis clinically; however, if lesions are non-specific or if the patient is immunosuppressed, this may not be possible.

Viral culture, looking for viral elements such as DNA or antigen, can be taken from sampling lesions or from fluids such as the cerebrospinal fluid (as in the diagnosis of herpes simplex encephalitis). Detecting DNA by PCR testing is a sensitive method.

4. Treatment

Management will depend on the site affected. Simple mouthwashes may soothe irritation of oral mucosa. Persistent or severe symptoms may require oral antivirals. Those unable to tolerate oral intake may need admission for IV fluids.

The antivirals aciclovir, famciclovir and valaciclovir may be used; all shorten lesion duration on skin and mucosa as well as reducing symptom length. They can also be used to reduce risk of relapse in oral or genital disease. If used, these agents should be initiated as early as possible.

Genital herpes can be treated using oral antivirals. Consider contact tracing and advising barrier contraception, but bear in mind that not all lesions may be covered by a condom.

Patients who have recurrent attacks should also be offered psychological support, as some may have relationship problems as a result of this condition. It is also wise to make patients aware they are potentially infectious when lesions are visible and that they can shed virus even in the absence of symptoms.

Neonatal infections and suspected encephalitis should be considered emergencies requiring urgent, same-day referral to secondary care.